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Long-term potentiation (LTP) and long-term depression (LTD) are considered to be cellular models suitable for studying the synaptic changes that likely occur during learning and memory. LTP has distinct phases, a transient protein synthesis-independent stage (early-LTP) followed under distinct circumstances by a late, longlasting and protein synthesis-dependent stage (late-LTP). In hippocampal CA1 neurons, LTP in either the apical or basal dendrites differ in their molecular requirement during induction as well as the setting of the tag, for example CaM kinase II mediates the setting of the tag in stratum radiatum but in basal dendrites (stratum oriens) the setting of the tag is mediated by either protein kinase A or protein kinase M zeta (Sajikumar et al. 2007). It has been reported that the late-LTP in the CA1 stratum radiatum requires the synergistic activation of different neurotransmitters during its induction (Frey 1997, Frey and Morris 1998). From this background we now investigated whether the LTP in stratum oriens requires similar or other synergistic interactions of different modulatory systems when compared with the stratum radiatum. Our preliminary studies using different selective antagonists of distinct modulatory transmitters systems revealed that late-LTP in basal dendrites is different with respect to its requirements for its induction when compared with late-LTP in apical CA1-dendrites.
Long-term potentiation (LTP) and long-term depression (LTD) of excitatory synaptic transmission are widespread phenomena expressed at many excitatory synapses in the mammalian brain. Because of its long duration, input specifi city and associative properties, LTP and LTD have been used as cellular models for memory. We wanted to investigate whether different locations on the apical dendritic branch could infl uence the induction of LTD and its related properties. Late-LTD could be induced in the apical CA1 dendrites by strong low-frequency stimulation (SLFS) pattern if the synapses were located distally, whereas, proximally located synapses were not able to maintain late-LTD. However, SLFS in both locations was able to trigger the synthesis of plasticity-related proteins, which could be evidenced by cross tagging experiments. In addition, we have investigated if hippocampal CA1-LTP prevents/occludes the establishment of LTD in the same synaptic input at specifi c time points after LTP-induction. We show induction of LTP occludes longer-lasting but not short-term LTD about 1 h after LTP-induction. However, after 4 h, i.e. after transformation of early- into late-LTP, also later forms of LTD can again be induced in the same synaptic input. Our results demonstrate that hippocampal neurons do not lose their capacity for the induction of longer forms of LTP or LTD after the establishment of late-LTP in the apical dendrites of hippocampal CA1- neurons.
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